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99Tc-MDP通过miR-338-3p靶向下调RANKL抑制破骨细胞活性机制研究 |
99Tc-MDP inhibiting the activity of osteoclast through miR-338-3p down-regulating RANKL |
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DOI:10.3969/j.issn.1006-7108.2020.02.004 |
中文关键词: 99Tc-MDP miR-338-3p RANKL 破骨细胞 骨质疏松 |
英文关键词:99Tc-MDP miR-338-3p RANK osteoclast osteoporosis |
基金项目:云南省科技厅-昆明医科大学联合专项基金(2018NS0243);云南省卫生科技计划项目(2018NS0243) |
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中文摘要: |
目的 探究99Tc-MDP通过miR-338-3p调控RANKL影响破骨细胞活性进而缓解骨质疏松发生的分子机制。方法 经药物处理细胞后,通过qRT-PCR检测破骨细胞(osteoporosis-derived osteoclast,OC)中miR-338-3p以及破骨细胞活性标志物CD51和MMP-9的表达;采用CCK-8、双荧光素酶报告基因和Western blotting检测OC细胞存活率、细胞增殖活力以及miR-338-3p与RANKL之间的靶向调节关系。结果 99Tc-MDP抑制OC细胞存活及CD51和MMP-9的表达;99Tc-MDP上调miR-338-3p同时下调RANKL;双荧光素酶报告基因以及Western blotting结果证实miR-338-3p靶向下调RANKL;进一步实验表明,99Tc-MDP通过上调miR-338-3p进而抑制RANKL表达从而抑制OC细胞增殖及活性。结论 99Tc-MDP通过上调miR-338-3p从而下调RANKL抑制破骨细胞活性,进而缓解骨质疏松发生。 |
英文摘要: |
Objective To explore the molecular mechanism of 99Tc-MDP alleviating osteoporosis through miR-338-3p to regulate RANKL to affect the activity of osteoclast (OC). Methods After the cells were treated by 99Tc-MDP, the expression of miR-338-3p and OC cells activity marker CD51 and MMP-9 were detected by qRT-PCR. CCK-8 assay, dual luciferase reporter gene assay and Western blotting were used to detect the proliferation, livability of OC and the targeted relationship of miR-338-3p and RANKL. Results 99Tc-MDP inhibited the expression of OC cells activity marker CD51 and MMP-9 and suppressed the livability of OC cells. 99Tc-MDP could up-regulate miR-338-3p and down-regulate RANKL. The results of dual luciferase reporter gene assay and Western blotting suggested that miR-338-3p could target RANKL and down-regulate it. Furthermore, 99Tc-MDP inhibited the proliferation and activity of OC cells through inhibiting RANKL by up-regulating miR-338-3p. Conclusion 99Tc-MDP alleviates osteoporosis by inhibiting the activity of osteoclast through miR-338-3p down-regulating RANKL. |
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